Osteochondritis dissecans, or OCD, is the most clinically important manifestation of osteochondrosis, and is a major problem in the equine industry. Grondahl, A. M., The incidence of osteochondrosis in the tibiotarsal joint of Norwegian Standardbred trotters; Eq. Vet. Sci. 11:273-274 (1991); and Jeffcott, L. B., Osteochondrosis in the horse--searching for the key to pathogenesis, Eq. Vet. J. 23:331-338 (1991). Radiographic evidence of osteochondrotic lesions reduces the perceived potential for optimal performance, and therefore, the value of young horses. Gaustad G., et al., Lameness in three-year-old Standardbred trotters--influence of parameters determined during the first year of life; J. Eq. Vet. Sci. 15:233-239 (1995); Laws, E. G., et al., Racing performance of Standardbreds after conservative and surgical treatment for tarsocrural osteochondrosis; Eq. Vet. J. 25:199-202 (1993); and McIllwraith, C. W., et al., Osteochondritis dissecans of the tarsocrural joint: results of treatment with arthroscopic surgery; Eq. Vet. J. 23:155-162 (1991); and McIllwraith, C. W., What is developmental orthopedic disease, osteochondrosis, osteochondritis, metabolic bone disease?; Proc. 39th Am. Assoc. Eq. Practitioners, pp. 35-44 (1993). Osteochondritis dissecans has been identified as a contributing factor in catastrophic breakdowns in racehorses, which are detrimental to public perception and acceptance of racing sports. Krook, K., et al., Fractures in Thoroughbred racehorses; Cornell Vet. 78, (Suppl.) 11:5-133 (1988).
Osteochondritis dissecans is very common in Standardbred horses and primarily affects the hock. Hoppe, F., Radiological investigations of osteochondrosis dissecans in Standardbred trotters and Swedish Warmblood horses; Eq. Vet. J. 16:425-429 (1984); and McIllwraith, C. W., et al., Osteochondritis dissecans of the tarsocrural joint: results of treatment with arthroscopic surgery; Eq. Vet. J. 23:155-162 (1991). Lesions usually develop in horses between three to twelve months of age, with new lesions rarely appearing in horses over a year old, although clinical signs of lameness may not appear until the horse is put into work. Jeffcott, L. B., Osteochondrosis in the horse--searching for the key to pathogenesis; Eq. Vet. J. 23:331-338 (1991). Multiple causes have been proposed for osteochondritis dissecans, including genetics, trauma, endocrine/metabolism, and nutrition. Williams, M. A., et al., Developmental orthopedic disease: minimizing the incidence of a poorly understood disorder; The Compendium 15:859-872 (1993).
A genetic predisposition to osteochondritis dissecans has been well documented in the Standardbred horse. Gaustad G., et al., Lameness in three-year-old Standardbred trotters--influence of parameters determined during the first year of life; J. Eq. Vet. Sci. 15:233-239 (1995); and Schougaard, et al., A radiological survey of tibiotarsal osteochondrosis in a selected population of trotting horses in Denmark and its possible genetic significance; Eq. Vet. J. 22:288-289 (1990); Grondahl, et al., Heritability estimations of osteochondrosis in the tibiotarsal joint and bony fragments in the palmar/plantar portion of the metacarpo- and metatarsophalangeal joints of horses; J. Am. Vet. Med. Assoc. 203:101-104 (1993); and Philipson, J., et al., Osteochondrosis in the tarsocrural joint and osteochondral fragments in the fetlock joints in Standardbred Trotters II: Heritability; Eq. Vet. J. (Suppl.) 16:38-41 (1993). However, because the nature of the hereditary defect which increases the risk of osteochondritis dissecans in horses has not been identified, a suitable genetic screen is unavailable.
Another proposed factor in the development of osteochondritis dissecans is the type of ration fed to young (&lt;1 year old) horses. Jeffcott, L. B., Osteochondrosis in the horse--searching for the key to pathogenesis; Eq. Vet. J. 23:331-338 (1991). For example, high grain rations are thought to be a potential cause of osteochondritis dissecans. However, not all young horses fed large amounts of grain develop osteochondritis dissecans. Glade, M. J., et al., A dietary etiology for osteochondrotic cartilage; J. Eq. Vet. Sci. 6:151-155 (1986); and Lewis, L. D., Equine Clinical Nutrition; Williams and Wilkins, Philadelphia, Pa., pp. 50-51, 429-433 (1995).
Ingestion of grain concentrate results in significant elevations in blood glucose and insulin concentration. Ralston, S. L., et al., Plasma glucose and insulin concentrations and feeding behavior in ponies; J. Animal Sci. 54:1132-1137 (1982). It has been postulated that such elevations in plasma insulin concentration may alter cartilage growth by influencing growth hormone and somatomedin release. Glade, M. J., The control of cartilage growth in osteochondrosis: a review; J. Eq. Vet. Sci. 65:175-187 (1986). It also has been hypothesized that osteochondritis dissecans may be associated with postprandial hyperglycemia and hyperinsulinemia and the resultant changes in thyroxine and growth hormone release. However, a definitive link between glucose intolerance and osteochondritis dissecans development has not previously been established. Glade, M. J., The control of cartilage growth in osteochondrosis: a review; J. Eq. Vet. Sci. 6:175-187 (1986); Glade, M. J., et al., A dietary etiology for osteochondrotic cartilage; Eq. Vet. Sci. 6:151-155 (1986).
Postprandial acidemia also may be influenced by insulin release. Glade, M. J., et al., A dietary etiology for osteochondrotic cartilage; Eq. Vet. Sci. 6:151-155 (1986). Postprandial acidemia is associated with enhanced urinary excretion of calcium, and possibly results from increased rates of bone resorption. Ralston, S. L., Dietary carbohydrates, acid base status and urinary calcium and phosphorus excretion in horses; Proc. 13th Equine Nutrition and Physiology Symposium, Gainesville, Fla., p. 42 (1993); and Wall, D. L., Dietary cation-anion balance, Eq. Vet. Data 12:17 (1991). Ingestion of grain concentrates by yearling horses reduces (p&lt;0.01) venous pH (i.e., venous base excess and bicarbonate concentrations) in proportion to the amount ingested. Ralston, S. L., Comparison of digestion and growth in yearlings fed high versus low grain rations; J. Animal Sci. 72, Suppl. 1:262 (1994). Moreover, both an excess and a deficiency of zinc have been associated with the development of osteochondritis dissecans in young horses. Lewis, L. D., Equine Clinical Nutrition, Williams and Wilkins, Philadelphia, Pa., pp. 50-51, 429-433 (1995). Zinc can potentiate the synthesis and hypoglycemic action of insulin. Anderson, L., et al., Nutrition in health and disease, 17th Ed. J. B. Lippincott Company, Philadelphia, Pa., pp. 88-90 (1992).
Thus, numerous studies have investigated the possible causes of osteochondritis dissecans with a number of hypotheses resulting. In spite of this research and the deleterious impact of the disease on horses and horse racing, a test for diagnosing a predisposition for equine osteochondritis dissecans has not previously been developed.